ArticleCancer research2010
The human WRN and BLM RecQ helicases differentially regulate cell proliferation and survival after chemotherapeutic DNA damage.
Article in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
49 citing papers in PubMed, 78 citations in OpenAlex.
- Homozygosity for the WRN Helicase-Inactivating Variant, R834C, does not confer a Werner syndrome clinical phenotype.Scientific reports · 2017Trial
- Dissecting the genotype in syndromic intellectual disability using whole exome sequencing in addition to genome-wide copy number analysis.Human genetics · 2013Trial
- G-quadruplex structures as regulators of cellular processes and drivers of genome instability in cancer.Critical reviews in biochemistry and molecular biology · 2026Review
- Structure of human lymphoid-specific helicase HELLS in its autoinhibited state.Nucleic acids research · 2026Article
- Unraveling syndrome-driven osteosarcoma: genetic insights and therapeutic frontiers.Orphanet journal of rare diseases · 2026Review
- BLM and FANCJ role in the response to G-quadruplex-dependent telomeric replicative stress.Communications biology · 2026Article
- Structure of human lymphoid-specific helicase HELLS in its autoinhibitory state.bioRxiv : the preprint server for biology · 2025Article
- How DNA secondary structures drive replication fork instability.DNA repair · 2025Review
- A Rare Presentation of Five Primary Cancers in a Patient With Werner Syndrome: A Case Report and Literature Review.Cureus · 2025Article
- Development of a Prognostic Risk Model Based on Oxidative Stress-related Genes for Platinum-resistant Ovarian Cancer Patients.Recent patents on anti-cancer drug discovery · 2025Article
- Response to Replication Stress and Maintenance of Genome Stability by WRN, the Werner Syndrome Protein.International journal of molecular sciences · 2024Review
- Replication stress as a driver of cellular senescence and aging.Communications biology · 2024Review
- Article
- Downregulation of BLM RecQ helicase inhibits proliferation, promotes the apoptosis and enhances the sensitivity of bladder cancer cells to cisplatin.Molecular medicine reports · 2022Article
- RecQ Helicase Somatic Alterations in Cancer.Frontiers in molecular biosciences · 2022Review
- Identifying novel SMYD3 interactors on the trail of cancer hallmarks.Computational and structural biotechnology journal · 2022Article
- USP37 regulates DNA damage response through stabilizing and deubiquitinating BLM.Nucleic acids research · 2021Article
- Synthetic Lethal Interactions of RECQ Helicases.Trends in cancer · 2021Review
- Functions of BLM Helicase in Cells: Is It Acting Like a Double-Edged Sword?Frontiers in genetics · 2021Review
- Heterozygous germlineProceedings of the National Academy of Sciences of the United States of America · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Loss-of-function mutations in the human RecQ helicase genes WRN and BLM respectively cause the genetic instability/cancer predisposition syndromes Werner syndrome and Bloom syndrome. To identify common and unique functions of WRN and BLM, we systematically analyzed cell proliferation, cell survival, and genomic damage in isogenic cell lines depleted of WRN, BLM, or both proteins. Cell proliferation and survival were assessed before and after treatment with camptothecin, cis-diamminedichloroplatinum(II), hydroxyurea, or 5-fluorouracil. Genomic damage was assessed, before and after replication arrest, by gamma-H2AX staining, which was quantified at the single-cell level by flow cytometry. Cell proliferation was affected strongly by the extent of WRN and/or BLM depletion, and more strongly by BLM than by WRN depletion (P = 0.005). The proliferation of WRN/BLM-codepleted cells, in contrast, did not differ from BLM-depleted cells (P = 0.34). BLM-depleted and WRN/BLM-codepleted cells had comparably impaired survival after DNA damage, whereas WRN-depleted cells displayed a distinct pattern of sensitivity to DNA damage. BLM-depleted and WRN/BLM-codepleted cells had similar, significantly higher gamma-H2AX induction levels than did WRN-depleted cells. Our results provide new information on the role of WRN and BLM in determining cell proliferation, cell survival, and genomic damage after chemotherapeutic DNA damage or replication arrest. We also provide new information on functional redundancy between WRN and BLM. These results provide a strong rationale for further developing WRN and BLM as biomarkers of tumor chemotherapeutic responsiveness.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.